SlTDP1 Is Required To Specify Tapetum Identity And For The Regulation Of Redox Homeostasis In Tomato Anthers

ABSTRACTThe tapetum is a specialized layer of cells within the anther adjacent to the sporogenic tissue. During its short life, it provides nutrients, molecules and materials to the pollen mother cells and microsporocytes being essential during callose degradation and pollen wall formation. However, the acquisition of tapetal cell identity in tomato plants is a process still poorly understood. We report here the identification and characterization of SlTPD1 (Solanum lycopersicum TPD1), a gene specifically required for pollen development in tomato plants. Gene editing was used to generate loss-of-function Sltpd1 mutants that showed absence of tapetal tissue. In these plants, sporogenous cells developed but failed to complete meiosis resulting in complete male sterility. Transcriptomic analysis conducted in wild-type and mutant anthers at an early stage revealed the down regulation of a set of genes related to redox homeostasis. Indeed, Sltpd1 anthers showed a reduction of reactive oxygen species (ROS) accumulation at early stages and altered activity of ROS scavenging enzymes. The obtained results highlight the importance of ROS homeostasis in the interaction between the tapetum and the sporogenous tissue in tomato plants.One sentence summaryThe small protein SlTPD1 is required for tapetum formation in tomato, highlighting the role of this tissue in the regulation of redox homeostasis during male gametogenesis.

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PsEND1 Is a Key Player in Pea Pollen Development Through the Modulation of Redox Homeostasis

Frontiers in Plant Science ◽

10.3389/fpls.2021.765277 ◽

2021 ◽

Vol 12 ◽

Author(s):

Rim Hamza ◽

Edelín Roque ◽

Concepción Gómez-Mena ◽

Francisco Madueño ◽

José Pío Beltrán ◽

...

Keyword(s):

Pollen Development ◽

Redox Homeostasis ◽

Functional Characterization ◽

Redox Balance ◽

Regulatory Elements ◽

Specific Gene ◽

Ros Scavenging ◽

Specific Expression ◽

Promoter Deletion Analysis ◽

Scavenging Enzymes

Redox homeostasis has been linked to proper anther and pollen development. Accordingly, plant cells have developed several Reactive Oxygen Species (ROS)-scavenging mechanisms to maintain the redox balance. Hemopexins constitute one of these mechanisms preventing heme-associated oxidative stress in animals, fungi, and plants. Pisum sativum ENDOTHECIUM 1 (PsEND1) is a pea anther-specific gene that encodes a protein containing four hemopexin domains. We report the functional characterization of PsEND1 and the identification in its promoter region of cis-regulatory elements that are essential for the specific expression in anthers. PsEND1 promoter deletion analysis revealed that a putative CArG-like regulatory motif is necessary to confer promoter activity in developing anthers. Our data suggest that PsEND1 might be a hemopexin regulated by a MADS-box protein. PsEND1 gene silencing in pea, and its overexpression in heterologous systems, result in similar defects in the anthers consisting of precocious tapetum degradation and the impairment of pollen development. Such alterations were associated to the production of superoxide anion and altered activity of ROS-scavenging enzymes. Our findings demonstrate that PsEND1 is essential for pollen development by modulating ROS levels during the differentiation of the anther tissues surrounding the microsporocytes.

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Possible Role of the Ca2+/Mn2+ P-Type ATPase Pmr1p on Artemisinin Toxicity through an Induction of Intracellular Oxidative Stress

Molecules ◽

10.3390/molecules24071233 ◽

2019 ◽

Vol 24 (7) ◽

pp. 1233 ◽

Cited By ~ 2

Author(s):

Onnicha Pongwattanakewin ◽

The Phyu ◽

Suchanya Suesattayapirom ◽

Laran Jensen ◽

Amornrat Jensen

Keyword(s):

Efflux Pump ◽

Manganese Content ◽

Artemisinin Resistance ◽

Protein Glycosylation ◽

Yeast Cells ◽

Loss Of Function ◽

Ros Scavenging ◽

Functional Homolog ◽

Ros Accumulation ◽

P Type

Artemisinins are widely used to treat Plasmodium infections due to their high clinical efficacy; however, the antimalarial mechanism of artemisinin remains unresolved. Mutations in P. falciparum ATPase6 (PfATP6), a sarcoplasmic endoplasmic reticulum Ca2+-transporting ATPase, are associated with increased tolerance to artemisinin. We utilized Saccharomyces cerevisiae as a model to examine the involvement of Pmr1p, a functional homolog of PfATP6, on the toxicity of artemisinin. Our analysis demonstrated that cells lacking Pmr1p are less susceptible to growth inhibition from artemisinin and its derivatives. No association between sensitivity to artemisinin and altered trafficking of the drug efflux pump Pdr5p, calcium homeostasis, or protein glycosylation was found in pmr1∆ yeast. Basal ROS levels are elevated in pmr1∆ yeast and artemisinin exposure does not enhance ROS accumulation. This is in contrast to WT cells that exhibit a significant increase in ROS production following treatment with artemisinin. Yeast deleted for PMR1 are known to accumulate excess manganese ions that can function as ROS-scavenging molecules, but no correlation between manganese content and artemisinin resistance was observed. We propose that loss of function mutations in Pmr1p in yeast cells and PfATP6 in P. falciparum are protective against artemisinin toxicity due to reduced intracellular oxidative damage.

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Silicon dioxide nanoparticles alleviate the threats of broomrape infection in tomato by inducing cell wall fortification and modulating ROS homeostasis

Environmental Science Nano ◽

10.1039/c9en01255a ◽

2020 ◽

Vol 7 (5) ◽

pp. 1415-1430

Author(s):

Mahmoud M. Y. Madany ◽

Ahmed M. Saleh ◽

Talaat H. Habeeb ◽

Wael N. Hozzein ◽

Hamada AbdElgawad

Keyword(s):

Cell Wall ◽

Silicon Dioxide ◽

Seed Priming ◽

Enzymatic Antioxidants ◽

Silicon Dioxide Nanoparticles ◽

Tomato Plants ◽

Ros Homeostasis ◽

Scavenging Enzymes

An infographic diagram that summarizes the influence of SiNP-seed priming upon tomato plants under Orobanche infection conditions. GRW: growth, PHO: photosynthesis, NEAO: non-enzymatic antioxidants, ASE: antioxidant-scavenging enzymes.

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Impact of Wheat Streak Mosaic Virus on Peroxisome Proliferation, Redox Reactions, and Resistance Responses in Wheat

International Journal of Molecular Sciences ◽

10.3390/ijms221910218 ◽

2021 ◽

Vol 22 (19) ◽

pp. 10218

Author(s):

Lidiya Mishchenko ◽

Taras Nazarov ◽

Alina Dunich ◽

Ivan Mishchenko ◽

Olga Ryshchakova ◽

...

Keyword(s):

Mosaic Virus ◽

Redox Homeostasis ◽

Field Trials ◽

Wheat Streak Mosaic Virus ◽

Peroxisome Proliferation ◽

Ros Scavenging ◽

Virus Content ◽

Pathogen Response ◽

Scavenging Enzymes ◽

The Impact

Although peroxisomes play an essential role in viral pathogenesis, and viruses are known to change peroxisome morphology, the role of genotype in the peroxisomal response to viruses remains poorly understood. Here, we analyzed the impact of wheat streak mosaic virus (WSMV) on the peroxisome proliferation in the context of pathogen response, redox homeostasis, and yield in two wheat cultivars, Patras and Pamir, in the field trials. We observed greater virus content and yield losses in Pamir than in Patras. Leaf chlorophyll and protein content measured at the beginning of flowering were also more sensitive to WSMV infection in Pamir. Patras responded to the WSMV infection by transcriptional up-regulation of the peroxisome fission genes PEROXIN 11C (PEX11C), DYNAMIN RELATED PROTEIN 5B (DRP5B), and FISSION1A (FIS1A), greater peroxisome abundance, and activation of pathogenesis-related proteins chitinase, and β-1,3-glucanase. Oppositely, in Pamir, WMSV infection suppressed transcription of peroxisome biogenesis genes and activity of chitinase and β-1,3-glucanase, and did not affect peroxisome abundance. Activity of ROS scavenging enzymes was higher in Patras than in Pamir. Thus, the impact of WMSV on peroxisome proliferation is genotype-specific and peroxisome abundance can be used as a proxy for the magnitude of plant immune response.

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Putrescine Depletion Affects Arabidopsis Root Meristem Size by Modulating Auxin and Cytokinin Signaling and ROS Accumulation

International Journal of Molecular Sciences ◽

10.3390/ijms22084094 ◽

2021 ◽

Vol 22 (8) ◽

pp. 4094

Author(s):

Ahmed M. Hashem ◽

Simon Moore ◽

Shangjian Chen ◽

Chenchen Hu ◽

Qing Zhao ◽

...

Keyword(s):

Linear Trend ◽

Primary Root ◽

Auxin Signaling ◽

Hormone Signaling ◽

Loss Of Function ◽

Ros Scavenging ◽

Cytokinin Signaling ◽

Auxin Distribution ◽

Ros Accumulation ◽

Phenotype Analysis

Polyamines (PAs) dramatically affect root architecture and development, mainly by unknown mechanisms; however, accumulating evidence points to hormone signaling and reactive oxygen species (ROS) as candidate mechanisms. To test this hypothesis, PA levels were modified by progressively reducing ADC1/2 activity and Put levels, and then changes in root meristematic zone (MZ) size, ROS, and auxin and cytokinin (CK) signaling were investigated. Decreasing putrescine resulted in an interesting inverted-U-trend in primary root growth and a similar trend in MZ size, and differential changes in putrescine (Put), spermidine (Spd), and combined spermine (Spm) plus thermospermine (Tspm) levels. At low Put concentrations, ROS accumulation increased coincidently with decreasing MZ size, and treatment with ROS scavenger KI partially rescued this phenotype. Analysis of double AtrbohD/F loss-of-function mutants indicated that NADPH oxidases were not involved in H2O2 accumulation and that elevated ROS levels were due to changes in PA back-conversion, terminal catabolism, PA ROS scavenging, or another pathway. Decreasing Put resulted in a non-linear trend in auxin signaling, whereas CK signaling decreased, re-balancing auxin and CK signaling. Different levels of Put modulated the expression of PIN1 and PIN2 auxin transporters, indicating changes to auxin distribution. These data strongly suggest that PAs modulate MZ size through both hormone signaling and ROS accumulation in Arabidopsis.

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Ascorbic Acid Modulation by ABI4 Transcriptional Repression of VTC2 in The Salt Tolerance of Arabidopsis

10.21203/rs.3.rs-116368/v1 ◽

2020 ◽

Author(s):

Xiamusiya Kakan ◽

Yanwen Yu ◽

Shenghui Li ◽

Xiaoying Li ◽

Rongfeng Huang ◽

...

Keyword(s):

Ascorbic Acid ◽

Salt Stress ◽

Salt Tolerance ◽

Stress Responses ◽

Transcriptional Repression ◽

Early Stage ◽

Stress Sensitivity ◽

Loss Of Function ◽

Ros Scavenging ◽

Plant Salt Tolerance

Abstract Background:Abscisic acid (ABA) plays an important role in plant abiotic stress responses, and ABA INSENSITIVE 4 (ABI4) is a pivotal transcription factor in the ABA signaling pathway. In Arabidopsis, ABI4 negatively regulates salt tolerance; however, the mechanism through which ABI4 regulates plant salt tolerance is poorly understood. Our previous study showed that ABI4 directly binds to the promoter of the VITAMIN C DEFECTIVE 2 (VTC2) gene, inhibiting the transcription of VTC2 and ascorbic acid (AsA) biosynthesis.Results: In the present study, we found that treatment with exogenous AsA could alleviate salt stress sensitivity of ABI4-overexpressing transgenic plants. The decreased AsA content and increased reactive oxygen species (ROS) levels in ABI4-overexpressing seedlings under salt treatment indicated that AsA-promoted ROS scavenging was related to ABI4-mediated salt tolerance. Gene expression analysis showed that ABI4 was induced at the early stage of salt stress, giving rise to reduced VTC2 expression. Accordingly, the abundance of the VTC2 protein decreased under the same salt stress conditions, and was absent in the ABI4 loss-of-function mutants, suggesting that the transcriptional inhibition of ABI4 on VTC2 resulted in the attenuation of VTC2 function. In addition, other encoding genes in the AsA biosynthesis and recycling pathways showed different responses to salt stress, demonstrating that AsA homeostasis is complicated under salinity stress. Conclusions: This study elucidates the negative modulation of ABI4 in salt stress tolerance through the regulation of AsA biosynthesis and ROS accumulation in plants.

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Ascorbic acid modulation by ABI4 transcriptional repression of VTC2 in the salt tolerance of Arabidopsis

BMC Plant Biology ◽

10.1186/s12870-021-02882-1 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Xiamusiya Kakan ◽

Yanwen Yu ◽

Shenghui Li ◽

Xiaoying Li ◽

Rongfeng Huang ◽

...

Keyword(s):

Ascorbic Acid ◽

Salt Stress ◽

Salt Tolerance ◽

Stress Responses ◽

Transcriptional Repression ◽

Early Stage ◽

Stress Sensitivity ◽

Loss Of Function ◽

Ros Scavenging ◽

Plant Salt Tolerance

Abstract Background Abscisic acid (ABA) plays an important role in plant abiotic stress responses, and ABA INSENSITIVE 4 (ABI4) is a pivotal transcription factor in the ABA signaling pathway. In Arabidopsis, ABI4 negatively regulates salt tolerance; however, the mechanism through which ABI4 regulates plant salt tolerance is poorly understood. Our previous study showed that ABI4 directly binds to the promoter of the VITAMIN C DEFECTIVE 2 (VTC2) gene, inhibiting the transcription of VTC2 and ascorbic acid (AsA) biosynthesis. Results In the present study, we found that treatment with exogenous AsA could alleviate salt stress sensitivity of ABI4-overexpressing transgenic plants. The decreased AsA content and increased reactive oxygen species (ROS) levels in ABI4-overexpressing seedlings under salt treatment indicated that AsA-promoted ROS scavenging was related to ABI4-mediated salt tolerance. Gene expression analysis showed that ABI4 was induced at the early stage of salt stress, giving rise to reduced VTC2 expression. Accordingly, the abundance of the VTC2 protein decreased under the same salt stress conditions, and was absent in the ABI4 loss-of-function mutants, suggesting that the transcriptional inhibition of ABI4 on VTC2 resulted in the attenuation of VTC2 function. In addition, other encoding genes in the AsA biosynthesis and recycling pathways showed different responses to salt stress, demonstrating that AsA homeostasis is complicated under salinity stress. Conclusions This study elucidates the negative modulation of ABI4 in salt stress tolerance through the regulation of AsA biosynthesis and ROS accumulation in plants.

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ROS Defense Systems and Terminal Oxidases in Bacteria

Antioxidants ◽

10.3390/antiox10060839 ◽

2021 ◽

Vol 10 (6) ◽

pp. 839

Author(s):

Vitaliy B. Borisov ◽

Sergey A. Siletsky ◽

Martina R. Nastasi ◽

Elena Forte

Keyword(s):

Defense Mechanisms ◽

Protective Role ◽

Superoxide Dismutases ◽

Oxygen Species ◽

Ros Scavenging ◽

Terminal Oxidases ◽

Defense Systems ◽

Respiratory Chains ◽

Scavenging Enzymes

Reactive oxygen species (ROS) comprise the superoxide anion (O2·−), hydrogen peroxide (H2O2), hydroxyl radical (·OH), and singlet oxygen (1O2). ROS can damage a variety of macromolecules, including DNA, RNA, proteins, and lipids, and compromise cell viability. To prevent or reduce ROS-induced oxidative stress, bacteria utilize different ROS defense mechanisms, of which ROS scavenging enzymes, such as superoxide dismutases, catalases, and peroxidases, are the best characterized. Recently, evidence has been accumulating that some of the terminal oxidases in bacterial respiratory chains may also play a protective role against ROS. The present review covers this role of terminal oxidases in light of recent findings.

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Somatic production of reactive oxygen species does not predict its production in sperm cells across Drosophila melanogaster lines

BMC Research Notes ◽

10.1186/s13104-021-05550-7 ◽

2021 ◽

Vol 14 (1) ◽

Author(s):

Biz R. Turnell ◽

Luisa Kumpitsch ◽

Anne-Cécile Ribou ◽

Klaus Reinhardt

Keyword(s):

Reactive Oxygen Species ◽

Drosophila Melanogaster ◽

Reactive Oxygen ◽

Future Research ◽

Ros Production ◽

Oxygen Species ◽

Loss Of Function ◽

Wild Type ◽

Ros Scavenging ◽

Transport Chain

Abstract Objective Sperm ageing has major evolutionary implications but has received comparatively little attention. Ageing in sperm and other cells is driven largely by oxidative damage from reactive oxygen species (ROS) generated by the mitochondria. Rates of organismal ageing differ across species and are theorized to be linked to somatic ROS levels. However, it is unknown whether sperm ageing rates are correlated with organismal ageing rates. Here, we investigate this question by comparing sperm ROS production in four lines of Drosophila melanogaster that have previously been shown to differ in somatic mitochondrial ROS production, including two commonly used wild-type lines and two lines with genetic modifications standardly used in ageing research. Results Somatic ROS production was previously shown to be lower in wild-type Oregon-R than in wild-type Dahomey flies; decreased by the expression of alternative oxidase (AOX), a protein that shortens the electron transport chain; and increased by a loss-of-function mutation in dj-1β, a gene involved in ROS scavenging. Contrary to predictions, we found no differences among these four lines in the rate of sperm ROS production. We discuss the implications of our results, the limitations of our study, and possible directions for future research.

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Altered Expression of Peroxiredoxins in Mouse Model of Progressive Myoclonus Epilepsy upon LPS-Induced Neuroinflammation

Antioxidants ◽

10.3390/antiox10030357 ◽

2021 ◽

Vol 10 (3) ◽

pp. 357

Author(s):

Mojca Trstenjak Prebanda ◽

Petra Matjan-Štefin ◽

Boris Turk ◽

Nataša Kopitar-Jerala

Keyword(s):

Mouse Model ◽

Redox Homeostasis ◽

Underlying Mechanism ◽

Loss Of Function ◽

Altered Expression ◽

Lps Challenge ◽

Progressive Myoclonus Epilepsy ◽

Myoclonus Epilepsy ◽

The Brain ◽

Deficient Mice

Stefin B (cystatin B) is an inhibitor of endo-lysosomal cysteine cathepsin, and the loss-of-function mutations in the stefin B gene were reported in patients with Unverricht–Lundborg disease (EPM1), a form of progressive myoclonus epilepsy. Stefin B-deficient mice, a mouse model of the disease, display key features of EPM1, including myoclonic seizures. Although the underlying mechanism is not yet completely clear, it was reported that the impaired redox homeostasis and inflammation in the brain contribute to the progression of the disease. In the present study, we investigated if lipopolysaccharide (LPS)-triggered neuroinflammation affected the protein levels of redox-sensitive proteins: thioredoxin (Trx1), thioredoxin reductase (TrxR), peroxiredoxins (Prxs) in brain and cerebella of stefin B-deficient mice. LPS challenge was found to result in a marked elevation of Trx1 and TrxR in the brain and cerebella of stefin B deficient mice, while Prx1 was upregulated only in cerebella after LPS challenge. Mitochondrial peroxiredoxin 3 (Prx3), was upregulated also in the cerebellar tissue lysates prepared from unchallenged stefin B deficient mice, while after LPS challenge Prx3 was upregulated in stefin B deficient brain and cerebella. Our results imply the role of oxidative stress in the progression of the disease.

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